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Medicine PART 1 > ACS > Flashcards

ACS Flashcards

1
Q

ACS - definition

A

Refers to a spectrum of acute myocardial ischaemia and/or infarction. Decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies. 3 conditions: - unstable angina - NSTEMI - STEMI

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2
Q

Stable vs Unstable Angina

A
  • Stable angina = at least 70% stenosis; chest pain only on exertion (supplies tissue at rest but heart needs to work harder on exertion) - Unstable angina = usually rupture of plaque with thrombosis -> subendocardial ischaemia. Pain at REST
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3
Q

ACS - cardiac tissue involvement

A
  • UA = subendocardial ischaemia - NSTEMI = subendocardial infarction (20-40 min after onset) - STEMI = transmural infaction (3-6 h after onset)
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4
Q

Cardiac biomarkers and ECG changes

A

UA - no changes in cardiac markers - ECG may be normal or have changes (ST depression, T wave inversion NSTEMI - elevated cardiac markers - ECG changes: ST depression, T wave inversion STEMI - elevated cardiac biomarkers - ECG changes: ST elevation of at least 1 mm in 2 or more contiguous leads, may have new LBBB or pathological Q waves

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5
Q

Cardiac biomarkers in ACS

A
  • Troponins (I and T): increase 3-12h from onset, peak at about 24-48 h and overall last 10-14 days - CK-MB: rises after 3 h, peaks at about 24 h and lasts up to 72 h (more useful to determine re-infarction) - myoglobin: first one to rise so useful for rapid Dx
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6
Q

ACS - risk factors

A
  • Increasing age - Gender (male for STEMI, female for UA) - Diabetes - Smoking - Hypertension - Hx of coronary artery disease - Hyperlipidaemia - PVD - CKD - Obesity - Inflammatory conditions e.g. RA
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7
Q

What is type 2 MI and some causes?

A

MI not due to atheroma - Supply and demand mismatch – cardiac muscle not receiving enough oxygen, often due to subendothelial tissue hypoxia – better prognosis than type 1 MI. Causes: - Anaemia - Hypoxia - Shock - Tachyarrhythmia - Bradyarrhythmia

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8
Q

What is type 3 MI?

A

Type 3 MI: sudden cardiac death due to thromboembolism (no time to measure cardiac enzyme therefore classified as type 3 MI as unknown if they had previous atheroma)

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9
Q

UA - presentation

A
  • increasing frequency of chest pain (several times a day, instead of occasionally) - increasing severity of chest pain (decreasing levels of activity needed to trigger pain and may occur at rest) - retrosternal pressure or heaviness radiating to jaw, arm, or neck that is improved by nitrates - dyspnoea - 4th heart sound (Indicates reduced myocardial relaxation due to ischaemia)
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10
Q

Acute MI - presentation

A
  • central crushing chest pain (sensation of tightness, heaviness, aching, burning, pressure, or squeezing) - diaphoresis, pallor - dyspnoea - N and/or V - dizziness or light-headedness - weakness and anxious - tachycardia - may have S3 or S4 heart sounds
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11
Q

Rarer causes of MI

A
  • Aortic dissection – tearing pain that radiates to the back, different bp in the different arms, widening of mediastinum, risk of pericardial effusion and tamponade - Coronary artery spasm - Oesophageal rupture - Pericarditis – saddle shaped ST elevation
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12
Q

ACS - investigations

A
  • ECG - cardiac biomarkers (tropinin, CK-MB +/- myoglobin) - FBC (normal or low Hb) - U+Es / electrolytes (usually normal) - blood glucose - lipid profile (normal or high total cholesterol and LDL) - coagulation profile (should be normal) - CXR (excludes HF, PE, aortic dissection, etc) - consider echo (regional wall motion abnormalities)
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13
Q

ACS - criteria for hospital admission

A

Suspected acute coronary syndrome (ACS), who: - Have current chest pain - Have signs of complications (such as PE) - Are pain-free, but have had chest pain in the last 12 hours and have an abnormal ECG - A recent history of ACS, and they develop further chest pain.

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14
Q

Stable angina - treatment (not ACS)

A
  • GTN spray (for use before performing activities known to cause symptoms of angina) - BB or CCB OR either one of: a long-acting nitrate (isosorbide mononitrate) Nicorandil Ivabradine Ranolazine - antiplatelet treatment (low dose aspirin - 75 mg daily) - statins
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15
Q

What to give to people with angina and: 1. stroke 2. diabetes

A

STROKE clopidogrel instead of aspirin (long term ischaemic stroke Rx also includes warfarin) DIABETES consider adding ACEi

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16
Q

ACS - immediate management

A

IMMEDIATE - Supplemental Oxygen - use a simple face mask. Adjust the flow rate to 5–10 L/min to achieve a target SpO2 of 94–98%. -Treat pain with glyceryl trinitrate (GTN spray) and/or opioid (for example IV diamorphine 2.5 mg to 5.0 mg) - Give aspirin 300 mg. Send a written record with the person that aspirin has been given. - Take a resting 12-lead ECG. Send the results to the hospital

17
Q

UA - further management (after MONA)

A
  • antiplatelet therapy (clopidogrel or prasugrel or ticagrelor) - BB or CCB - anticoagulant (heparin -unfractionated- or a low molecular weight heparin, or fondaparinux sodium) - glycoprotein IIb/IIIa inhibitors (eptifibatide) for high risk pts - consider ACEi if HTN persists after BB - chest pain not resolved: consider IV nitrates
18
Q

NSTEMI - further management (after MONA)

A
  • antiplatelet therapy (clopidogrel or prasugrel or ticagrelor) - BB or CCB Assess need for invasive or conservative approach 1. Invasive: PCI + anticoagulant (heparin -unfractionated- or a low molecular weight heparin, or fondaparinux sodium) +/- glycoprotein IIb/IIIa inhibitors (eptifibatide) 2. conservative = anticoagulation only
19
Q

STEMI - definitive management (haemodynamically stable)

A

PCI - gold standard - performed within 90 min of diagnosis - should also receive anticoagulant -> either heparin (unfractionated) or a LMWH (e.g. enoxaparin sodium) or bivalirudin to prevent clotting during the procedure - no-reflow or a thrombotic complication -> glycoprotein IIb/IIIa inhibitors (eptifibatide) > 90 min –> thrombolytic therapy - alteplase or reteplase - PCI after thrombolysis recommended in high-risk pts - + anticoagulation For both cases (additional Rx): aspirin, antiplatelet therapy (clopidogrel or prasugrel or ticagrelor), BB, statin, ezetimibe (if require additional lowering of LDL after statin)

20
Q

STEMI - definitive management (haemodynamically unstable)

A

1st line- PCI 2nd line - coronary artery bypass graft (CABG) + anticoagulation + aspirin + antiplatelet - no-reflow or a thrombotic complication -> glycoprotein IIb/IIIa inhibitors (eptifibatide)

21
Q

What is PCI?

A

Percutaneous coronary intervention (PCI or angioplasty with stent) 1. A catheter is fed via radial or femoral artery to the coronary artery for angiogram to locate the thrombus 2. A deflated balloon attached to a catheter (a balloon catheter) is passed over a guide-wire into the narrowed vessel and then inflated to a fixed size. 3. The balloon forces expansion of the blood vessel and the surrounding muscular wall, allowing an improved blood flow. 4. A stent may be inserted at the time of ballooning to ensure the vessel remains open, and the balloon is then deflated and withdrawn.

22
Q

ACS - lifestyle measures (2ary prevention)

A

Cardiac Rehabilitation Programme - exercise, education, relaxation and emotional support In addition to adequate control of HTN, DM, and hyperlipidaemia, risk-factor intervention includes: - smoking cessation - regular physical activity with 30 minutes of moderate-intensity aerobic activity at least 5 times/week - a healthy diet (low salt intake, decreased intake of saturated fats, regular intake of fruit and vegetables) - weight reduction

23
Q

ACS - long term management (2ary prevention)

A
  • low dose aspirin continued indefinitely (75 mg daily) - clopidogrel (or alternative) for 12 months - BB - statin - ACEi Consider angiotensin II antagonist eg valsartan if intolerant to ACEi; consider aldosterone antagonist and anticoagulants (for high risk or recurrence only) (remember CRABS = clopidogrel, ramipril, aspirin, BB, statin)
24
Q

Other causes of acute chest pain (NICE)

A
  • pulmonary embolism - tension pneumothorax - sudden-onset cardiac arrhythmia - cardiac tamponade - aortic dissection - ruptured oesophagus
25
Q

MI - complications

A
  • complication of Rx: bleeding (eg intracranial hrg, - complication of Rx: thrombocytopenia - congestive HF - ventricular arrhythmias eg VT and VF - BBB, heart block - acute mitral regurgitation (from rupture of papillary muscle) - VSD (from septal rupture) - acute pericardial tamponade (from ventricular free wall rupture) - post-infarction pericarditis (Dressler’s syndrome) - recurrent ischaemia and infarction - cardiac arrest
26
Q

Anterior MI’s show most in which leads? Which artery is affected?

A

V1-V4 Left anterior decending

27
Q

Inferior MI’s show most in which leads? Which artery is affected?

A

II, III, aVF Right coronary

28
Q

How do posterior MI’s present on an ECG?

A

Tall R waves in V1-V2 Possible ST depression (not elevation) in V1-V4 (reciprocal change)

29
Q

Lateral MI’s show most in which leads? Which artery is affected?

A

I, aVL, V5, V6 Left circumflex artery

30
Q

Within 48 hours of an MI a patient presents with signs of LVF, dropping BP and a new murmur, what is most likely diagnosis?

A

Papillary muscle rupture / MR (or ventricular septal rupture)

31
Q

What are the criteria for PCI in suspected ACS? (3 things on ECG and time criteria)

A
  • ST elevation (2mm in anterior leads, 1mm in I,II,III,avF) - Any new LBBB - Posterior changes (ST depression + big R waves in V1-V3) - Must be within 12 hours of symptom onset
32
Q

What is the grace score?

A

Estimates admission-6 month mortality for patients with ACS. Based on: age heart rate systolic blood pressure renal function congestive heart failure ST-segment deviation cardiac arrest elevated biomarkers 6 Month Estimated Mortality eg 1 to 69 Points = less than 1% - Low risk <1.5% - High risk >9%

33
Q

Primary prevention of CVD

A

Lifestyle factors: - smoking - alcohol - diet - physical activity - weight management Lipid modification therapy (offered when CV risk > 10%) - 1st line: atorvastatin 20 mg - 2nd line: Ezetimibe

Medicine PART 1 (8 decks)

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